Logo - Rejuvenal
Rheumatoid arthritis and Osteo arthritis
Joints without pain
Arthritis is an inflammatory process that destroys joint tissue. It affects millions of people worldwide. There are many different forms of arthritis, the most common being rheumatoid arthritis and osteoarthritis.
Rheumatoid arthritis is a condition of localized autoimmunity, which causes the destruction of the synovial membrane (which produces synovial fluid) and the cartilage within joints. Without lubrication and the cushioning provided by cartilage, the joint becomes very painful to move. Pain and inflammation, along with stiffness, characterize rheumatoid arthritis. The initial symptoms of rheumatoid arthritis are enlargement of the joints in the fingers, with increasing pain and loss of function as the disease flares up. Eventually, bone erodes away, and conventional doctors usually recommend joint replacement surgery.
Although the exact mechanism of arthritis is not known, it is known that viral and bacterial infections can lead to the condition. Certain hereditary factors have also been linked to arthritis. Destruction of joints is caused by the release of substances from immune cells which usually attack foreign organisms, but turn against joint tissue instead. Immune cells are provoked into the area by pro-inflammatory cytokines and certain prostaglandins. These substances cause the destruction of joint tissue by increasing the production of enzymes and cells which break down the tissue. It is thought that free radicals play a part in the process since pro-inflammatory cytokines cause the release of these destructive molecules.
FlexPro® is a very advanced supplement for the treatment of inflamed joints such as is the case with Rheumatoid Arthritis. Where for Osteo Arthritis FlexMatrix® is a very good choise, inflammed joints have the need for a different treatment. FlexMatrix® is specially reformulated for this purpose. Besides the already proven capability to restoring cartilage in joints, it now also contains very strong phytonutrients to reduce the inflammatory proces. Using FlexPro will reduce joint pain in just weeks of time. During this time it is also recommended to reduce the intake of Omega-6 fatty acids and increase the intake of Omega-3, preferably EPA and DHA. OmegaMatrix is an ideal product to do so. Mostly after one month patients can switch to the regular FlexMatrix. Although only in rare cases, if the inflammation continues to happen, it is better to stay on the FlexPro® for a longer period of time. 4 tablets a day is a very good doses, but in some very extreme painful cases, the doses can be doubled up to 8 tablets a day. Use between 3 to 4 grams of OmegaMatrix® per day for the increase of anti inflammatory prostaglandins. Reduce or even limit the intake of ALL Omega 6 vegetable oils and red meat. The use of good quality, extra vergin olive oil is recommended.
Oral administration of type II collagen suppresses non-specifically induced chronic arthritis in rats.
Yoshino S. Biomed Pharmacother. 1996;50(1):24-8.
Department of Microbiology, Saga Medical School, Japan.
The present study was designed to investigate the efficacy of oral administration of type II collagen (CII)(Cartidea®) on non-specifically induced chronic arthritis in rats, induced by intra-articular injection of a mineral oil, squalene (synthetic, not from fish or plant resource). When CII was fed before injection of squalene, no chronic arthritis developed. Feeding CII after the induction of arthritis was also effective in suppressing the progression of chronic joint inflammation. Lymph node cells from rats with squalene-induced arthritis failed to show proliferative responses to CII. In rats fed and primed with CII, there was a decrease in proliferative responses to CII. Arthritis induced by the mineral oil was markedly suppressed by the spleen cells from animals fed CII. These results indicate that non-specifically induced arthritis may be downregulated by the oral administration of CII and that the downregulation of joint inflammation may be due to the generation of CII-specific regulatory T cells that react to CII abundance in cartilage.
Read below some studies to back up the anti inflammatory ingredients used in this powerful formulation.
Cat's Claw, Bowelia Serrata, Pomegranate, Green Tea Extract, Vitamin Ester C, Curcumin
Coffee, tea, and caffeine consumption and risk of rheumatoid arthritis: results from the Iowa Women's Health Study.
Mikuls TR, Cerhan JR, Criswell LA, Merlino L, Mudano AS, Burma M, Folsom AR, Saag KG.
University of Alabama at Birmingham, 35294-3296, USA. Arthritis Rheum. 2002
OBJECTIVE: To evaluate whether coffee, tea, and caffeine consumption are risk factors for rheumatoid arthritis (RA) onset among older women.
METHODS: These factors were evaluated in a prospective cohort study that was initiated in 1986 and that included 31,336 women ages 55-69 years without a history of RA. Risk factor data were self-reported using a mailed questionnaire. Through 1997, 158 cases of RA were identified and validated against medical records. The relative risk (RR) and 95% confidence interval (95% CI) were used as the measures of association and were adjusted for age, alcohol use, smoking history, age at menopause, marital status, and the use of hormone replacement therapy.
RESULTS: Compared with those reporting no use, subjects drinking > or =4 cups/day of decaffeinated coffee were at increased risk of RA (RR 2.58, 95% CI 1.63-4.06). In contrast, women consuming >3 cups/day of tea displayed a decreased risk of RA (RR 0.39, 95% CI 0.16-0.97) compared with women who never drank tea. Caffeinated coffee and daily caffeine intake were not associated with the development of RA. Multivariable adjustment for a number of potential confounders did not alter these results. The associations of RA onset with the highest categories of decaffeinated coffee consumption (RR 3.10, 95% CI 1.75-5.48) and tea consumption (RR 0.24, 95% CI 0.06-0.98) were stronger in women with seropositive disease compared with those with seronegative disease (RR 1.54, 95% CI 0.62-3.84 and RR 0.93, 95% CI 0.27-3.20, respectively).
CONCLUSION: Decaffeinated coffee intake is independently and positively associated with RA onset, while tea consumption shows an inverse association with disease onset. Further investigations of decaffeinated coffee and tea intake as arthritis risk factors are needed to verify these findings and explore their biologic basis.
Turnover of type II collagen and aggrecan in cartilage matrix at the onset of inflammatory arthritis in humans: relationship to mediators of systemic and local inflammation.
Fraser A, Fearon U, Billinghurst RC, Ionescu M, Reece R, Barwick T, Emery P, Poole AR, Veale DJ. Arthritis Rheum. 2003 Nov;48(11):3085-95.
St. Vincents University Hospital, Dublin, Ireland.
OBJECTIVE: To determine in vivo the extent of damage to, and changes in turnover of, articular cartilage type II collagen (CII) and the proteoglycan aggrecan following the onset of inflammatory arthritis in humans, and to examine the hypothesis that there are direct relationships between cartilage biomarkers of damage/turnover and clinical, histologic, and molecular markers of inflammation.
METHODS: Synovial fluid (SF) and synovial membrane (SM) were obtained by arthroscopy, and a synovitis score was determined, in 32 patients with rheumatoid arthritis (RA) (13 with early untreated disease, 19 with established disease), 18 with psoriatic arthritis (PsA), and 10 with osteoarthritis (OA). Systemic disease activity markers were recorded, and SM CD3+ T cells, CD4+ T cells, CD68+ macrophages, and lining layer hyperplasia were quantified. SF levels of tumor necrosis factor alpha (TNFalpha), interleukin-10 (IL-10), matrix metalloproteinase 1 (MMP-1), MMP-3, Col2-3/4C(Long mono) neoepitope (C2C) (reflecting collagenase cleavage of cartilage CII), C-propeptide of type II procollagen (PIICP) (a biosynthesis marker), keratan sulfate (KS), and the 846 epitope of aggrecan (turnover) were measured by enzyme-linked immunosorbent assay or radioimmunoassay.
RESULTS: Levels of cartilage degradation products in early RA or early PsA were not elevated above levels in OA, although in early inflammatory arthritis, TNFalpha and MMP-1 levels were similar to those observed in late inflammatory disease and higher than those in OA. PIICP was reduced in early RA. Correlations were observed between the SF C2C neoepitope level and the Health Assessment Questionnaire score, C-reactive protein level, plasma viscosity, synovitis score, and SF TNFalpha and MMP-1 levels. KS epitope content was reduced in direct relation to SM macrophage infiltration in the sublining and lining layers and in the presence of elevated SF MMP-3. Both SF MMP-1 and SF MMP-3 levels correlated with CD4+ T cell infiltration and lining layer hyperplasia in the SM, and MMP-1 levels correlated with lining layer CD68 levels, but TNFalpha and IL-10 levels did not.
CONCLUSION: Except for CII synthesis, there were no significant changes in extracellular matrix turnover of aggrecan or CII in the early stages of human inflammatory arthritis. However, the direct correlation between the increases in TNFalpha and MMP-1 production and collagen degradation suggests that collagenase cleavage of cartilage collagen is related to the activities of TNFalpha and MMP-1. The reduction in CII synthesis in early RA may contribute to the developing pathology, since a lack of synthesis of this molecule would inhibit maintenance of cartilage matrix.
Hyaluronic acid